Pulseless electrical activity overview: Difference between revisions
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==Overview== | ==Overview== | ||
Pulseless electrical activity is defined as the absence of a pulse or cardiac contractility despite the presence of electrocardiographic activity. The most common causes are [[respiratory failure]] and [[hypovolemia]]. | Pulseless electrical activity is defined as the absence of a [[pulse]] or [[cardiac contractility]] despite the presence of [[electrocardiographic]] activity. The most common [[causes]] are [[respiratory failure]] and [[hypovolemia]], [[Hypoxia|'''H'''ypoxia]], [[Hydrogen|'''H'''ydrogen]] ions ([[Acidosis]]), [[Hypothermia|'''H'''ypothermia]][[Hyperkalemia|'''H'''yperkalemia]]or [[Hypokalemia|'''H'''ypokalemia]], [[Hypoglycemia|'''H'''ypoglycemia]], [[Tablets|'''T'''ablets]] or [[Toxins|'''T'''oxins]] ([[Drug overdose]]) such as [[beta blocker]]s, [[tricyclic antidepressant]]s, or [[calcium channel blockers]], [[Cardiac tamponade|'''T'''amponade]], [[Tension pneumothorax|'''T'''ension pneumothorax]], [[Thrombosis|'''T'''hrombosis]] ([[Myocardial infarction]]), [[Thrombosis|'''T'''hrombosis]] ([[Pulmonary embolism]]), [[Physical trauma|'''T'''rauma]] ([[Hypovolemia]] from [[blood loss]]), [[Covid-19]]. PEA is associated with a poor [[prognosis]], particularly if the underlying cause is not readily identifiable and treated. Absence of palpable [[pulse]] is the main finding. [[Echocardiogram]] can identify several rapidly reversible causes of PEA such as [[cardiac tamponade]], [[myocardial infarction]], [[cardiac rupture]] and underfilling of the ventricle due to [[hypovolemia]]. [[ECG]] findings shows [[sinus rhythm]] or [[sinus tachycardia]], with discernible [[P waves]] and [[QRS complexes]]. Sometimes there is a [[bradycardia]], with or without [[P waves]], and often there is a [[wide QRS complex]]. According to the current American Heart Association-[[Advanced Cardiac Life Support]] (AHA-ACLS) guidelines [[CPR]] is the mainstay of treatment in all [[patients]]. Administering 100% [[oxygen]] to reverse [[hypoxia]], [[Intubation|intubat]]<nowiki/>e the [[patient]], establishing [[IV]] access should be the priority. The mainstay of [[drug]] therapy for PEA is [[epinephrine]] 1mg every 3–5 minutes. Immediately after administering [[epinephrine]] attention should be directed to reverse any possible causes of PEA as they are the most common [[causes]] like [[hypovolemia]] (i.e. [[hypovolemic shock]]) which should be treated with [[IV fluids]]or [[packed red blood cell transfusion]]. | ||
==Historical Perspective== | ==Historical Perspective== | ||
Pulseless electrical activity as the main approach for [[sudden cardiac arrest]] (SCA) was not completely studied until the middle of the 1980's. The explanation for this, is that [[ventricular fibrillation]] (VF) and [[ventricular tachycardia]] (VT), were the main causes for the morbidity and mortality of SCA. However there has been a change in approaching the causes of SCA, pointing to PEA as the initial rhythm leading to SCA. | Pulseless electrical activity as the main approach for [[sudden cardiac arrest]] ([[SCA]]) was not completely studied until the middle of the 1980's. The explanation for this, is that [[ventricular fibrillation]] (VF) and [[ventricular tachycardia]] ([[VT]]), were the main causes for the morbidity and mortality of [[SCA]]. However there has been a change in approaching the causes of [[SCA]], pointing to PEA as the initial rhythm leading to [[SCA]]. | ||
==Pathophysiology== | ==Pathophysiology== | ||
PEA( pulseless electrical activity) usually occurs when an insult involves the cardiovascular, gastrointestinal or the respiratory | PEA( pulseless electrical activity) usually occurs when an insult involves the [[cardiovascular]], [[gastrointestinal]] or the [[Respiratory systems|respiratory system]]<nowiki/>s. Any such event can lead to decrease in [[cardiac contractility]], and the situation gets even worse by potential [[acidosis]], [[hypoxia]], and worsening [[vagal tone]]. A severe initial insult often reduces [[cardiac output]] which may in turn cause [[myocardial ischemia]], [[left ventricular failure]], [[hypoxia]] and [[metabolic acidosis]]. These [[Pathophysiology|pathophysiologic]] disturbances further reduce [[cardiac output]] further exacerbating the downward spiral with loss of [[cardiac output]]; [[hypotension]], [[loss of consciousness]] and [[apnea]] rapidly ensue. Other possible mechanisms for pulseless electrical activity include Elevated Afterload, Electromechanical Dissociation, Reduced Contractility, Parasympathetic theory. | ||
==Causes== | |||
Common causes of PEA include [[respiratory failure]] in 40% to 50% of cases, and [[hypovolemia]]. [[Hypovolemia|'''H'''ypovolemia]], [[Hypoxia|'''H'''ypoxia]], [[Hydrogen|'''H'''ydrogen]] ions ([[Acidosis]]), [[Hypothermia|'''H'''ypothermia]][[Hyperkalemia|'''H'''yperkalemia]]or [[Hypokalemia|'''H'''ypokalemia]], [[Hypoglycemia|'''H'''ypoglycemia]], [[Tablets|'''T'''ablets]] or [[Toxins|'''T'''oxins]] ([[Drug overdose]]) such as [[beta blocker]]s, [[tricyclic antidepressant]]s, or [[calcium channel blockers]], [[Cardiac tamponade|'''T'''amponade]], [[Tension pneumothorax|'''T'''ension pneumothorax]], [[Thrombosis|'''T'''hrombosis]] ([[Myocardial infarction]]), [[Thrombosis|'''T'''hrombosis]] ([[Pulmonary embolism]]), [[Physical trauma|'''T'''rauma]] ([[Hypovolemia]] from [[blood loss]]), [[Covid-19]]. | |||
==Differentiating Pulseless Electrical Activity from Other Diseases== | |||
PEA(Pulseless electrical activity) should be differentiated from [[asystole]], [[ventricular fibrillation]], [[Ventricular flutter]], [[Torsade de Pointes]]. In [[asystole]], there is cessation of any [[cardiac]] activity and lack of [[cardiac output]] on this basis. In [[Ventricular fibrillation]] there is no organized [[electrical]] activity present, while there are only fine fibrillatory waves. [[Peripheral arterial disease]] can also present with inability to feel a peripheral [[pulse]] so it should be differentiated based on other findings as well. | |||
==Epidemiology and Demographics== | |||
The [[incidence]] of [[SCA]] ranges between 300,000 to 370,000 cases per year, 50% of which are due to PEA. PEA accounts for approximately 20% of out-hospital cardiac arrests and for a third of the in-hospital cardiac arrests. There is a slight female preponderance for PEA in addition, PEA is associated with increased age and black race. | |||
==Risk Factors== | ==Risk Factors== | ||
The administration of [[beta blockers]] and [[calcium channel blockers]] is associated with an increased risk of PEA. This may be due to their effect on Ca / troponin interactions, and their inhibition of myocardial contractility. | The administration of [[beta blockers]] and [[calcium channel blockers]] is associated with an increased risk of PEA. This may be due to their effect on Ca / troponin interactions, and their inhibition of myocardial contractility. | ||
==Natural History, Complications and Prognosis== | ==Natural History, Complications and Prognosis== | ||
PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identifiable and treated. The presence of a [[QRS interval]] > 0.20 seconds is associated with a poorer prognosis. The survival of in hospital PEA is only 11.2%. | PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identifiable and treated. The presence of a [[QRS interval]] > 0.20 seconds is associated with a poorer prognosis. The survival of in hospital PEA is only 11.2%. The survival for out of hospital occurrence of PEA is higher (19.5%) than for in hospital PEA, likely due to the higher incidence of reversible causes among patients with out of hospital arrest. The survival of PEA as a presenting rhythm is poorer than [[ventricular tachycardia]] or [[ventricular fibrillation]]. | ||
==Diagnosis== | ==Diagnosis== | ||
===Diagnostic Study Of Choice=== | ===Diagnostic Study Of Choice=== | ||
===History and Symptoms=== | |||
Absence of palpable [[pulse]] is the main finding. Depending upon the cause of pulseless electrical activity the following might be found, [[Tracheal deviation]] or the unilateral absence of breath sounds in case of [[tension pneumothorax]], decreased [[skin]] turgor, Cool [[extremities]], [[Tachycardia]] in case of hypotension, traumatic [[chest]], , [[Cyanosis]] etc | |||
===Echocardiography=== | ===Echocardiography=== | ||
A rapid beside echocardiogram can identify several rapidly reversible causes of PEA such as [[cardiac tamponade]], [[myocardial infarction]], [[cardiac rupture]] and underfilling of the ventricle due to [[hypovolemia]]. Elevated right heart filling pressures suggest [[pulmonary embolism]]. [[Tension pneumothorax]] can also be observed on a bedside echocardiogram. | A rapid beside [[echocardiogram]] can identify several rapidly reversible [[causes]] of PEA such as [[cardiac tamponade]], [[myocardial infarction]], [[cardiac rupture]] and underfilling of the [[ventricle]] due to [[hypovolemia]]. Elevated [[right heart]] filling pressures suggest [[pulmonary embolism]]. [[Tension pneumothorax]] can also be observed on a bedside [[echocardiogram]]. | ||
===Laboratory Findings=== | ===Laboratory Findings=== | ||
Athough there are no [[diagnostic]] [[laboratory]] findings associated with PEA(pulseless electrical activity) testing should be ordered to rule out the most common reversible [[causes]] of PEA(pulseless electrical activity) like [[Hyperkalemia]] or [[Hypokalemia]], [[hypoxia]] and [[acidosis]] which can be seen with[[ABG]], [[exsanguination]] [[hematocrit]]. | Athough there are no [[diagnostic]] [[laboratory]] findings associated with PEA(pulseless electrical activity) testing should be ordered to rule out the most common reversible [[causes]] of PEA(pulseless electrical activity) like [[Hyperkalemia]] or [[Hypokalemia]], [[hypoxia]] and [[acidosis]] which can be seen with[[ABG]], [[exsanguination]] [[hematocrit]]. | ||
===Electrocardiogram=== | |||
The appearance of the [[electrocardiogram]] in the setting of PEA varies, but several common patterns exist. There may be a normal [[sinus rhythm]] or [[sinus tachycardia]], with discernible [[P waves]] and [[QRS complexes]]. Sometimes there is a [[bradycardia]], with or without [[P waves]], and often there is a [[wide QRS complex]]. The presence of a [[QRS interval]] > 0.20 seconds is associated with a poorer [[prognosis]]. The [[EKG]] should be carefully evaluated for signs of [[Hyperkalemia]], [[ST segment elevation MI]], [[hypothermia]], [[QRS interval]] prolongation suggests [[tricyclic antidepressant overdose]] | |||
===CT scan=== | |||
There are no [[CT scan]] findings associated with pulseless electrical activity. However it can be used to identify some of the [[causes]] of pulseless electrical activity like [[cardiac tamponade]], [[tension pneumothorax]].[[Superior vena cava]] and[[Inferior vena cava]] enlargement, [[Hepatic vein|Hepatic]] and [[renal vein]] enlargment, Periportal edema, Compression of [[coronary sinus]], Angulation of [[Ventricular septum|interventricular septum]],[[Pericardial]] thickening, Collapse of the [[right atrium]], [[Aorta|Aortic]] blood contrast level these are seen in [[cardiac tamponade]] [[CT]]. | |||
==Treatment== | ==Treatment== | ||
Latest revision as of 13:56, 13 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Maneesha Nandimandalam, M.B.B.S.[2]
Overview
Pulseless electrical activity is defined as the absence of a pulse or cardiac contractility despite the presence of electrocardiographic activity. The most common causes are respiratory failure and hypovolemia, Hypoxia, Hydrogen ions (Acidosis), HypothermiaHyperkalemiaor Hypokalemia, Hypoglycemia, Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers, Tamponade, Tension pneumothorax, Thrombosis (Myocardial infarction), Thrombosis (Pulmonary embolism), Trauma (Hypovolemia from blood loss), Covid-19. PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identifiable and treated. Absence of palpable pulse is the main finding. Echocardiogram can identify several rapidly reversible causes of PEA such as cardiac tamponade, myocardial infarction, cardiac rupture and underfilling of the ventricle due to hypovolemia. ECG findings shows sinus rhythm or sinus tachycardia, with discernible P waves and QRS complexes. Sometimes there is a bradycardia, with or without P waves, and often there is a wide QRS complex. According to the current American Heart Association-Advanced Cardiac Life Support (AHA-ACLS) guidelines CPR is the mainstay of treatment in all patients. Administering 100% oxygen to reverse hypoxia, intubate the patient, establishing IV access should be the priority. The mainstay of drug therapy for PEA is epinephrine 1mg every 3–5 minutes. Immediately after administering epinephrine attention should be directed to reverse any possible causes of PEA as they are the most common causes like hypovolemia (i.e. hypovolemic shock) which should be treated with IV fluidsor packed red blood cell transfusion.
Historical Perspective
Pulseless electrical activity as the main approach for sudden cardiac arrest (SCA) was not completely studied until the middle of the 1980's. The explanation for this, is that ventricular fibrillation (VF) and ventricular tachycardia (VT), were the main causes for the morbidity and mortality of SCA. However there has been a change in approaching the causes of SCA, pointing to PEA as the initial rhythm leading to SCA.
Pathophysiology
PEA( pulseless electrical activity) usually occurs when an insult involves the cardiovascular, gastrointestinal or the respiratory systems. Any such event can lead to decrease in cardiac contractility, and the situation gets even worse by potential acidosis, hypoxia, and worsening vagal tone. A severe initial insult often reduces cardiac output which may in turn cause myocardial ischemia, left ventricular failure, hypoxia and metabolic acidosis. These pathophysiologic disturbances further reduce cardiac output further exacerbating the downward spiral with loss of cardiac output; hypotension, loss of consciousness and apnea rapidly ensue. Other possible mechanisms for pulseless electrical activity include Elevated Afterload, Electromechanical Dissociation, Reduced Contractility, Parasympathetic theory.
Causes
Common causes of PEA include respiratory failure in 40% to 50% of cases, and hypovolemia. Hypovolemia, Hypoxia, Hydrogen ions (Acidosis), HypothermiaHyperkalemiaor Hypokalemia, Hypoglycemia, Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers, Tamponade, Tension pneumothorax, Thrombosis (Myocardial infarction), Thrombosis (Pulmonary embolism), Trauma (Hypovolemia from blood loss), Covid-19.
Differentiating Pulseless Electrical Activity from Other Diseases
PEA(Pulseless electrical activity) should be differentiated from asystole, ventricular fibrillation, Ventricular flutter, Torsade de Pointes. In asystole, there is cessation of any cardiac activity and lack of cardiac output on this basis. In Ventricular fibrillation there is no organized electrical activity present, while there are only fine fibrillatory waves. Peripheral arterial disease can also present with inability to feel a peripheral pulse so it should be differentiated based on other findings as well.
Epidemiology and Demographics
The incidence of SCA ranges between 300,000 to 370,000 cases per year, 50% of which are due to PEA. PEA accounts for approximately 20% of out-hospital cardiac arrests and for a third of the in-hospital cardiac arrests. There is a slight female preponderance for PEA in addition, PEA is associated with increased age and black race.
Risk Factors
The administration of beta blockers and calcium channel blockers is associated with an increased risk of PEA. This may be due to their effect on Ca / troponin interactions, and their inhibition of myocardial contractility.
Natural History, Complications and Prognosis
PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identifiable and treated. The presence of a QRS interval > 0.20 seconds is associated with a poorer prognosis. The survival of in hospital PEA is only 11.2%. The survival for out of hospital occurrence of PEA is higher (19.5%) than for in hospital PEA, likely due to the higher incidence of reversible causes among patients with out of hospital arrest. The survival of PEA as a presenting rhythm is poorer than ventricular tachycardia or ventricular fibrillation.
Diagnosis
Diagnostic Study Of Choice
History and Symptoms
Absence of palpable pulse is the main finding. Depending upon the cause of pulseless electrical activity the following might be found, Tracheal deviation or the unilateral absence of breath sounds in case of tension pneumothorax, decreased skin turgor, Cool extremities, Tachycardia in case of hypotension, traumatic chest, , Cyanosis etc
Echocardiography
A rapid beside echocardiogram can identify several rapidly reversible causes of PEA such as cardiac tamponade, myocardial infarction, cardiac rupture and underfilling of the ventricle due to hypovolemia. Elevated right heart filling pressures suggest pulmonary embolism. Tension pneumothorax can also be observed on a bedside echocardiogram.
Laboratory Findings
Athough there are no diagnostic laboratory findings associated with PEA(pulseless electrical activity) testing should be ordered to rule out the most common reversible causes of PEA(pulseless electrical activity) like Hyperkalemia or Hypokalemia, hypoxia and acidosis which can be seen withABG, exsanguination hematocrit.
Electrocardiogram
The appearance of the electrocardiogram in the setting of PEA varies, but several common patterns exist. There may be a normal sinus rhythm or sinus tachycardia, with discernible P waves and QRS complexes. Sometimes there is a bradycardia, with or without P waves, and often there is a wide QRS complex. The presence of a QRS interval > 0.20 seconds is associated with a poorer prognosis. The EKG should be carefully evaluated for signs of Hyperkalemia, ST segment elevation MI, hypothermia, QRS interval prolongation suggests tricyclic antidepressant overdose
CT scan
There are no CT scan findings associated with pulseless electrical activity. However it can be used to identify some of the causes of pulseless electrical activity like cardiac tamponade, tension pneumothorax.Superior vena cava andInferior vena cava enlargement, Hepatic and renal vein enlargment, Periportal edema, Compression of coronary sinus, Angulation of interventricular septum,Pericardial thickening, Collapse of the right atrium, Aortic blood contrast level these are seen in cardiac tamponade CT.
Treatment
Medical therapy
The current American Heart Association-Advanced Cardiac Life Support (AHA-ACLS) guidelines advise the following be undertaken in all patients start CPR immediately, administer 100% oxygen to reverse hypoxia,Intubate the patient, establish IV access.The mainstay of drug therapy for PEA is epinephrine 1mg every 3–5 minutes.Higher doses of epinephrine can be administered in patients with suspected beta blocker and calcium channel blocker overdose.Immediately after administering epinephrine attention should be directed to reverse any possible causes of PEA as they are the most common causes like hypovolemia (i.e. hypovolemic shock) which should be treated with IV fluidsor packed red blood cell transfusion. Others like electrolyte abnormalities including hyper/hypokalemia should be corrected immediately as they can be life threatening as well as tension pneumothorax.
Surgery
External and internal pacing have not been shown to improve outcome and are not recommended. There may be capture of the signals, but there is no improvement in contractility.